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. 2017 Aug 28;114(37):9900–9905. doi: 10.1073/pnas.1701757114

Fig. S3.

Fig. S3.

Effect of HRas on UPR pathways. (A) Immunoblots of JNK and p38 activation in primary and HRas keratinocytes at indicated time points. (B) Immunoblots of JNK, c-JUN, and ERK1/2 phosphorylation in keratinocytes expressing a doxycycline (Dox)-inducible HRasG12V 24 h after HRas induction. (C) Immunoblots showing activation of JNK pathway in primary keratinocytes by treatment with thapsigargin (Tg) for 90 min. (D) Immunoblots of p-PERK, PERK, p-eIF2a, and eIF2a in primary or HRas-transduced keratinocytes at indicated time points. (E) Relative levels of Atf4 and Chop mRNA in primary and HRas keratinocytes 5 d after transduction. (F) Relative level of ER stress target genes in primary keratinocytes (PK) transduced with shCTRL, and HRas keratinocytes cotransduced with shCTRL, shIRE1α, or shXBP1 lentivirus. Values are normalized to PK + shCTRL. In E and F, data represent mean ± SEM (n = 3). *P < 0.05 as determined by a Student’s t test. ns, nonsignificant; shCTRL, shcontrol.